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CHAPTER 14

Diagnosis and Management of Traumatic Atlanto-occipital


Dislocation Injuries
RECOMMENDATIONS
DIAGNOSTIC:
Standards: There is insufficient evidence to support diagnostic standards.
Guidelines: There is insufficient evidence to support diagnostic guidelines.
Options:
A lateral cervical x-ray is recommended for the diagnosis of atlanto-occipital dislocation. If a radiological
method for measurement is used, the basion-axial interval-basion-dental interval method is recommended.
The presence of upper cervical prevertebral soft tissue swelling on an otherwise nondiagnostic plain x-ray
should prompt additional imaging.
If there is clinical suspicion of atlanto-occipital dislocation, and plain x-rays are nondiagnostic, computed
tomography or magnetic resonance imaging is recommended, particularly for the diagnosis of non-Type II
dislocations.
TREATMENT:
Standards: There is insufficient evidence to support treatment standards.
Guidelines: There is insufficient evidence to support treatment guidelines.
Options: Treatment with internal fixation and arthrodesis using one of a variety of methods is recommended.
Traction may be used in the management of patients with atlanto-occipital dislocation, but it is associated
with a 10% risk of neurological deterioration.

RATIONALE

lthough traumatic atlanto-occipital dislocation (AOD)


is perceived to be an uncommon injury frequently
resulting in death, improvements in emergency management of the patient in the field, rapid transport, and better
recognition have resulted in more survivors of AOD in the
past 2 decades. Infrequent observation of patients with AOD
and missed diagnoses may impair outcomes of patients with
this unusual injury (44). An assimilation of the reported experiences of clinicians evaluating and managing AOD may
facilitate development of diagnostic and treatment options for
this traumatic disorder. Specific questions that were evaluated include the sensitivity of plain x-rays, computed tomography (CT), and magnetic resonance imaging (MRI) in the
diagnosis of AOD, as well as the safety and efficacy of various
treatment modalities for AOD, including no treatment, traction, external immobilization, and internal fixation with
fusion.

SEARCH CRITERIA
A computerized search of the National Library of Medicine
database of the literature published from 1966 to 2001 was
undertaken. The medical subject headings atlanto-occipital

joint and dislocation yielded 690 and 86,205 citations, respectively. A subset of 233 citations contained both headings.
The reference lists of the articles were reviewed to identify
additional case reports. Because fewer than 100 cases of survivors of AOD were identified, even single case reports were
considered, provided that basic inclusion criteria were met.
The articles were reviewed using the following criteria for
inclusion in diagnosis: human survivors, type of traumatic
atlanto-occipital dislocation, and plain radiographic findings.
The articles were also reviewed using the following criteria
for inclusion in treatment: human survivors, type of traumatic
AOD, management, and outcome. The observations from the
reports were combined because the usual methods for analysis were precluded by the infrequent observation of this injury. The type of dislocation was classified according to
Traynelis et al. (51) into Type I (anterior), Type II (longitudinal), and Type III (posterior) dislocations. Lateral, rotational,
and multidirectional dislocations that could not be classified
into one of these types were considered separately and are
noted as Other Type. The duration of follow-up ranged
from several weeks to 4 years. Of the articles meeting the
diagnostic selection criteria, 48 articles with 79 patients provided data on 29 Type I, 32 Type II, 4 Type III, and 14 other
types of AOD. Two of these articles (10, 44) included one

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Guidelines for Management of Cervical Spinal Injuries

patient each from two previously published individual case


reports (41, 42). Of the articles meeting the treatment selection
criteria, 43 articles with 62 patients provided data on 24 Type
I, 23 Type II, 3 Type III, and 12 other types of AOD. Two of
these articles (10, 44) included one patient each from two
previously published individual case reports (41, 42). All articles contained Class III medical evidence consisting of either
single case studies or small case series with no report containing more than six patients. The information provided by these
reports was compiled and scrutinized, and it constitutes the
basis for this guideline. Summaries of these reports are provided in Tables 14. 1 and 14.2.

SCIENTIFIC FOUNDATION
Diagnosis
A variety of radiographic measurements (17) have been
proposed for the diagnosis of AOD on a lateral cervical x-ray
(Fig. 14.1). A displacement of more than 10 mm between the
basion and dens is considered abnormal by Wholey et al. (53).
A ratio of the basion-posterior atlas arch distance to the
opisthion-anterior atlas arch distance of more than 1 is considered abnormal by Powers et al. (43). A distance of more
than 13 mm between the posterior mandible and anterior atlas
or 20 mm between the posterior mandible and dens is considered abnormal by Dublin et al. (12). Failure of a line from
the basion to the axis spinolaminar junction to intersect C2 or
a line from the opisthion to the posterior inferior corner of the
body of the axis to intersect C1 are considered abnormal by
Lee et al. (32). Finally, a displacement of more than 12 mm
or more than 4 mm between the basion and posterior C2
line, or a displacement of more than 12 mm from the basion to
dens (2 mm more than the Wholey recommendation) is considered abnormal by Harris et al. (24, 25). A comparative
study by Lee et al. (32) found a 50% sensitivity of the Wholey
method, 33% sensitivity of the Powers ratio, and a 25% sensitivity of the Dublin method. The authors applied their X-line
method with a 75% sensitivity (32). Although neither the
Powers ratio nor X-line method could be applied in nearly
half their patients, a comparative study by Harris et al. (25)
found a 60% sensitivity of the Powers ratio, a 20% sensitivity
of the Lee method, and 100% sensitivity of the basion-axial
interval-basion-dental interval (BAI-BDI) method among patients in whom the required landmarks could be identified.
Przybylski et al. (44) reported failure to diagnose AOD in two
of five patients with the Powers ratio, one of five patients with
the X-line method, and two of five patients with the BAI-BDI
method. No radiographic method reviewed has complete sensitivity. The BAI-BDI method proposed by Harris et al. (which
incorporates the basion-dens distance described by Wholey) is
at present the most reliable means to diagnose AOD on a
lateral cervical spine x-ray.
Many of the case reports and case series in the literature do
not describe the method(s) used for diagnosis of AOD. Because the most sensitive method was proposed by Harris et al.
(25) in 1994, this method was probably not used for many of
the evaluations. Although, retrospectively, a diagnosis was
possible on the first lateral x-ray in 60 of 79 patients (sensi-

tivity, 0.76), the diagnosis was actually made in only 45 of the


79 patients (sensitivity, 0.57) on the first lateral x-ray. Of the 15
patients whose diagnosis could have been made on the first
lateral x-ray, 3 were not stratified by type, whereas 11 of the
remaining 12 were not Type II dislocations (1, 7, 9, 13, 27, 29,
41, 44, 46, 49, 52, 54). A second lateral x-ray (nine cases),
tomography (one case), fluoroscopy (two cases), CT (two
cases), and MRI (five cases) were required for diagnosis in 19
of 79 patients (1, 3, 4, 8, 10, 1921, 26, 28, 36, 40, 4244). The
sensitivities stratified by type of dislocation are: Type I, 0.83
(24 of 29 patients); Type II, 0.72 (23 of 32 patients); Type III,
0.75 (3 of 4 patients), other type, 0.71 (10 of 14 patients).
Because these data were obtained from case reports and small
case series, comparison with the accuracy of plain x-rays in
patients without AOD could not be performed. As a result,
specificity, predictive values, and likelihood ratios cannot be
discerned from the available literature.
Of the 15 patients in whom the diagnosis was missed on the
initial plain x-rays, the initial neurological condition of 3
patients was unknown (1). Of the remaining 12 patients, 4
were neurologically normal (one Type I, one Type III, two
other type) (13, 29). Two of those four patients originally
reported as normal developed a monoparesis (one Type I, one
other type) (7, 49). Neither recovered completely. Eight of the
remaining 12 patients had neurological abnormalities from
the outset, five of whom worsened. Four of the five transiently
worsened, including one Type I injury patient with quadriparesis and Cranial Nerve IX, X, and XII palsies (9) who was
only spastic at last follow-up. One patient with a Type I injury
developed a hemiparesis but recovered (27). One Type I injury patient developed quadriparesis and was hemiparetic at
follow-up (46). One lateral dislocation patient with paraparesis and torticollis had recovered at last follow-up (52). One
patient (Type I) with initial monoparesis experienced permanent worsening and was quadriplegic at follow-up (54).
Although plain x-rays do not reliably identify AOD, the
index of suspicion may be increased with the identification of
prevertebral soft tissue swelling. Although plain x-rays were
obtained in all cases considered, the presence or absence of
soft tissue swelling was described in only half (1, 3, 4, 6, 911,
15, 19, 21, 22, 26, 27, 31, 3336, 38, 39, 42, 45, 48, 52, 54). The
sensitivity of soft tissue swelling is 0.90 (37 of 41 cases). Acute
craniocervical CT was performed in 40 of 79 patients with
AOD (14, 611, 20, 22, 2630, 33, 34, 38, 41, 42, 44, 45, 48, 52,
55). However, for 15 of 40 patients, the authors did not report
whether AOD was diagnosed by CT. The diagnosis of AOD
was made by CT in 21 of 25 patients (sensitivity, 0.84). Although no other computed tomographic findings were reported in 11 of 40 patients, 24 of the remaining 29 patients
with AOD studied with CT had hemorrhages (19 subarachnoid hemorrhages, 1 subdural hemorrhage, 4 contusions).
Five patients had no computed tomographic evidence of associated hemorrhage. Nine of 15 patients in whom the diagnosis of AOD was missed on the first plain x-ray had subsequent acute computed tomographic scanning; 8 had
subarachnoid or other associated hemorrhage (1, 9, 8, 44).
Craniocervical MRI was performed in 18 of 79 patients with
AOD (68, 10, 15, 21, 23, 26, 27, 30, 34, 37, 40, 42, 49, 55). The

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TABLE 14.1. Summary of Reports on Imaging Diagnosis of Atlanto-occipital Dislocation Injuriesa


Series (Ref. No.)
Grabb et al., 1999 (21)

AOD Type

Diagnosis Made by

X-ray Findings

CT Findings

MRI Findings

Plain x-ray

STS, Powers

Unreported

Partial tear tectorial membrane

II

Plain x-ray

STS, Powers

None performed

Tear posterior AOL

II

MRI

STS, Powers

None performed

Partial tear tectorial membrane

Naso et al., 1997 (37)

I/II

Plain x-ray

No mention STS

Unreported

Delayed study

Sponseller and Cass, 1997 (49)

Plain x-ray (missed)

No mention STS

None performed

None performed

II

Plain x-ray

No mention STS

Unreported

BS contusion

MRI

Powers/BDI/X-line

SAH, Dx

BS contusion, Dx

II

Plain x-ray (missed)

Powers/BDI/X-line

SAH, Dx

BS contusion, Dx

II

2nd plain x-ray

Powers/BDI /X-line

SAH, Dx

None performed

I/lateral

Plain x-ray (missed)

Powers/BDI/X-line

Normal, head only

None performed

I/lateral

Plain x-ray (missed)

Powers/BDI/X-line

SAH, Dx

None performed

Yamaguchi et al., 1996 (55)

Plain x-ray

No mention STS

SAH, tomography

BS contusion, Dx

Guigui et al., 1995 (22)

Plain x-ray

STS

Dx

None performed

Ahuja et al., 1994 (1)

Fluoroscopy

STS, Powers

SAH, unknown

None performed

5 plain x-ray (3

STS, Powers

None performed

None performed

Przybylski et al., 1996 (44)


Pang and Wilberger, 1980 (41)

II

missed)

Donahue et al., 1994 (11)

II

STS, Powers

SAH, Dx

None performed

II

STS, Powers

SAH, unknown

None performed

I/II

STS, Powers

None performed

None performed

I/II

STS, Powers

SAH, Dx

None performed

Plain x-ray

STS

None performed

None performed

II

Plain x-ray

STS, 5 mm distraction

None performed

None performed

II

Plain x-ray

STS

None performed

None performed

II

Plain x-ray

6 mm distraction

Intracerebral bleed

None performed

Palmer and Turney, 1994 (40)

II

CT

No mention STS

Unreported

Cord contusion, Dx

Dickman et al., 1993 (10)

II

Plain x-ray

15 mm distraction

None performed

None performed

Papadopoulos et al., 1991 (42)

Rotatory

CT

STS

Dx

None performed

Rotatory

MRI

STS

No blood, Dx

Epidural, Dx

II/rotatory

2nd plain x-ray

STS

Dx

Epidural, Dx

II

Plain x-ray

No mention STS

None performed

Dx

Hosono et al., 1993 (27)

Plain x-ray (missed)

STS

Edema, head only

Delayed study

Matava et al., 1993 (34)

II

Plain x-ray

STS

Delayed study

None performed

II

Plain x-ray

No mention STS

None, Dx

None performed

II

Plain x-ray

No mention STS

SAH, Dx

BS contusion

II

Plain x-ray

STS

BS contusion, Dx

None performed

II

Plain x-ray

STS

Dx

None performed

Plain x-ray

STS

SAH, Dx

SAH, Dx

Plain x-ray

STS, Powers/X-line

SAH

Dx

Farley et al., 1992 (15)

Plain x-ray

STS, Power

None performed

Cord contusion

Belzberg and Tranmer, 1991 (3)

II

2nd plain x-ray

STS

SAH, Dx

None performed

Hladky et al., 1991 (26)

II

MRI

No mention STS

Contusion, head only

Dx

II

MRI

No STS

Normal, head only

Dx

Lee et al., 1991 (33)

II

Plain x-ray

STS

SAH, Dx

None performed

I/rotatory

Plain x-ray

STS

Dx

None performed

Maves et al., 1991 (35)

II

Plain x-ray

No mention STS

None performed

None performed

Harmanli and Koyfman, 1993 (23)

Nischal et al., 1993 (38)


Bundshuh et al., 1992 (6)

Montane et al., 1991 (36)

II

Plain x-ray

No mention STS

None performed

None performed

III

Plain x-ray

No mention STS

None performed

None performed

Plain x-ray

STS

None performed

None performed

II

2nd plain x-ray

STS

None performed

None performed

II

2nd plain x-ray

No STS

None performed

None performed

Dibenedetto and Lee, 1990 (9)

Plain x-ray (missed)

STS

ICH, Dx

None performed

Jones et al., 1990 (30)

Plain x-ray

No mention STS

Dx

Premedullary edema

Colnet et al., 1989 (8)

Lateral rotatory

Tomography

Late study

SAH, Dx

Delayed study

Jevtich, 1989 (29)

Lateral

Plain x-ray (missed)

No mention STS

Delayed study

None performed

Hummel and Plave, 1988 (28)

2nd plain x-ray

No mention STS

Subdural, head only

None performed

Zampella et al., 1988 (56)

II

Plain x-ray

No mention STS

SAH, head only

Delayed study

Georgopoulos et al., 1987 (20)

Cineradiography

No mention STS

Delayed study

None performed

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TABLE 14.1. Continued


Series (Ref. No.)

AOD Type

Diagnosis Made by

X-ray Findings

CT Findings

MRI Findings

Plain x-ray

STS

SAH, Dx

None performed

III

2nd plain x-ray

No mention STS

None performed

None performed

Collalto et al., 1986 (7)

I/lateral

Plain x-ray (missed)

No STS

SAH, head only

Delayed study

Putnam et al., 1986 (45)

Plain x-ray

STS, Powers

SAH, Dx

None performed

Ramsay et al., 1986 (46)

Plain x-ray (missed)

No mention STS

None performed

None performed

Roy-Camille et al., 1986 (48)

Late plain x-ray

No mention STS

Delayed study

None performed

Plain x-ray

STS

None performed

None performed

Zigler et al., 1986 (57)

Plain x-ray

No mention STS

None performed

None performed

Watridge et al., 1985 (52)

Lateral

Plain x-ray (missed)

No STS

Delayed study

None performed

Banna et al., 1983 (2)

Rotatory

Plain x-ray

No mention STS

Dx

None performed

Kaufman et al., 1982 (31)

II

Plain x-ray

STS

None performed

None performed

II

Plain x-ray

STS

None performed

None performed

Woodring et al., 1981 (54)

Plain x-ray

No mention STS

None performed

None performed

Plain x-ray (missed)

STS

None performed

None performed

Powers et al., 1979 (43)

Plain x-ray

Late study

None performed

None performed

II

2nd plain x-ray

No mention STS

None performed

None performed

Rockswold and Seljeskog, 1979 (47)

II

Plain x-ray

No mention STS

None performed

None performed

Eismont and Bohlman, 1978 (13)

III

Plain x-ray (missed)

No mention STS

None performed

None performed

Fruin and Pirotte, 1977 (18)

Plain x-ray

No mention STS

None performed

None performed

Page et al., 1973 (39)

Plain x-ray

STS

None performed

None performed

Evarts, 1970 (14)

Plain x-ray

No mention STS

None performed

None performed

Gabrielsen and Maxwell, 1966 (19)

2nd plain x-ray

STS

None performed

None performed

Farthing, 1948 (16)

III

Plain x-ray

No mention STS

None performed

None performed

Bools and Rose, 1986 (4)

a
One patient was eliminated because the plain x-ray interpretation was not reported: Ferrara and Bartfield (17) (1 patient). Three articles were
eliminated because the type of dislocation was not reported: Georgopoulos et al. (20) (2 of 3 patients); Hladky et al. (26) (1 of 3 patients); Naso
et al. (37) (1 of 2 patients). One article (5 patients) was eliminated because individual patient data was not reported: Bulas et al. (5) (5 of 5
patients). AOD, atlanto-occipital dislocation; MRI, magnetic resonance imaging; CT, computed tomography; STS, soft tissue swelling; BDI,
basion-dental interval; SAH, subarachnoid hemorrhage; Dx, diagnosis. , done or positive; , not done or negative; BS, brainstem; ICH,
intracerebral hemorrhage; AOL, atlanto-occipital ligament.

MRI findings were not reported for 4 of the 18 patients studied. The diagnosis of AOD could be made in 12 of 14 cases
studied with MRI (sensitivity, 0.86).
In summary, physicians often miss the diagnosis of AOD on
plain x-rays (sensitivity, 0.57), particularly in the circumstance
of nonlongitudinal dislocations (non-Type II). Although improved interpretation may increase the sensitivity of plain
x-rays to 0.76, additional imaging of the craniovertebral junction with CT or MRI is recommended in patients suspected of
having AOD, given their superior sensitivity over plain
x-rays. Other methods, such as fluoroscopy, tomography, and
myelography, have also been used to confirm the diagnosis of
AOD. Neurological abnormalities, including lower cranial
nerve paresis (particularly Cranial Nerves VI, X, and XII),
monoparesis, hemiparesis, quadriparesis, respiratory dysfunction including apnea, and complete high cervical cord
motor deficits in the setting of normal plain spinal x-rays
should prompt additional imaging with CT or MRI. The presence of prevertebral soft tissue swelling on plain x-rays and
subarachnoid hemorrhage at the craniovertebral junction on
computed tomographic scans should prompt consideration of
the diagnosis of AOD (5, 44).

Treatment
Ten patients in the literature did not receive initial treatment for AOD, nine of whom were not correctly diagnosed

until neurological worsening occurred (7, 8, 10, 20, 46, 48, 49,
52, 54). Five of the nine patients had Type I injuries, and four
of the nine had other injury types. Four of nine had persistent
deficits at last follow-up that were worse in comparison with
their examinations on presentation (7, 10, 49, 54). Two of these
patients were normal initially. At last follow-up, one had a
Cranial Nerve X deficit with spasticity (Type I) (49), and one
had monoparesis (7). The other two patients had mild initial
deficits. One patient with an initial Cranial Nerve VI palsy
had hemiparesis at last follow-up (10), and another with
initial monoparesis was quadriplegic at follow-up (54). Five
patients who worsened initially without treatment eventually
improved from their initial neurological condition. Finally,
one quadriplegic patient with Type II AOD (56) who was not
treated improved to quadriparesis at last follow-up. In summary, failure to treat AOD resulted in worsening of all patients with incomplete injuries. Nearly half of these patients
failed to improve to their initial examination baseline
conditions.
Of 21 patients with AOD initially treated with traction, 2
worsened transiently and developed worsening quadriparesis
and Cranial Nerve VI deficits. Both patients had resolution of
their Cranial Nerve VI deficits but not of their quadriparesis
with discontinuation of traction. One patient had a Type II
injury (40), and one patient had a rotational dislocation (10).
Four patients were initially normal and remained normal at

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TABLE 14.2. Summary of Reports on Treatment of Atlanto-occipital Dislocation Injuriesa


Series (Ref. No.)

Type

Initial Examination

Treatment

Outcome

Naso et al., 1997 (37)

Mixed I/II

Quadriplegia

Supportive

Sponseller and Cass, 1997 (49)

Normal

None (neuro worse), traction, fusion brace

Death 5 wk
Spastic, CN 10

II

Normal

Brace failed (6 wk), fusion

Normal

Przybylski et al., 1996 (44)

Quadriplegia

Collar fusion

Quadriplegia

Pang and Wilberger, 1980 (41)

II

Quadriplegia

Halo failed (22 wk), fusion

Quadriplegia
CN 10

II

Normal

Fusion collar

Mixed I/lateral

Hemiplegia

Collar fusion

Monoparesis

Mixed I/lateral

Quadriparesis, CN 6/7/12

Fusion collar

CN 12

Yamaguchi et al., 1996 (55)

Quadriplegia, CN 10, 11, 12

Brace failed (10 wk), fusion

Quadriplegia, CN 10, 11, 12

Guigui et al., 1995 (22)

Normal

Fusion brace

Normal

Donahue et al., 1994 (11)

Hemiparesis

Halo distracted (temporarily neuro worse),

Hyperreflexic

fusion
II

CN 6

Halo fusion

Normal

II

Quadriplegia, CN 7/10

Collar/traction fusion

Quadriparesis, CN 7/10
Quadriparesis

II

Quadriparesis, CN 3/7

Fusion

Palmer and Turney, 1994 (40)

II

Quadriparesis, CN 6

Traction (neuro worse), brace fusion

Quadriparesis

Dickman et al., 1993 (10)

II

Quadriplegia, CN 9/10

Brace

Unchanged (sepsis, death at 3 mo)

Papadopoulos et al., 1991 (42)

Rotatory

Quadriparesis, CN 6

Traction (neuro worse), fusion halo

Quadreparesis

Rotatory

CN 6

None (neuro worse), fusion halo

Hemiparesis

Mixed II/rotatory

Hemiparesis, CN 3/6

Halo fusion

Normal

Harmanli and Koyfman, 1993 (23)

II

Hemiparesis, CN 12

Fusion brace

Normal

Hosono et al., 1993 (27)

Hemiparesis

Brace (neuro worse), fusion brace

Normal

Matava et al., 1993 (34)

II

Hemiplegia, CN 6/12

Fusion brace

Spastic, CN 6

II

Hemiparesis, CN 6

Fusion brace

Normal

II

CN 6/9/10

Fusion brace

Spastic

II

Quadriparesis, CN 3, 6, 9, 10

Brace fusion

Hemiparesis, CN 3, 6, 9, 10

II

Quadriplegia, CN 9, 10

Brace fusion

Hemiparesis

Bundshuh et al., 1992 (6)

Quadriparesis, CN 6, 9, 10, 12

Traction fusion

CN 6, 12

Farley et al., 1992 (15)

Quadriplegia, CN 10

Traction brace

Quadriplegia

Belzberg and Tranmer, 1991 (3)

II

Quadriparesis, CN 6, 9, 10

Traction brace fusion

Monoparesis, CN 6

Lee et al., 1991 (33)

II

Normal

Traction fusion

Normal

Mixed I/rotatory

CN 6

Brace fusion

CN 6

Hemiparesis

Fusion brace

Spastic

II

Quadriparesis

Traction, fusion brace

Normal

Nischal et al., 1993 (38)

Montane et al., 1991 (36)

II

Quadriplegia

Fusion brace

Quadriplegia

Dibenedetto and Lee, 1990 (9)

Quadriparesis, CN 9, 10, 12

Collar (neuro worse, 6 wk), fusion brace

Spastic

Colnet et al., 1989 (8)

Mixed lateral/rotatory

Hemiplegia, CN 6, 9, 10

None (neuro worse), traction shunt

Hemiparesis

decompression
Jevtich, 1989 (29)

Lateral

Normal

Traction brace

Hummel and Plaue, 1988 (28)

Hemiparesis

Fusion brace

Normal

Zampella et al., 1988 (56)

II

Quadriplegia, CN 512

None

Quadriplegia, CN 6

Georgopoulos et al., 1987 (20)

Normal

None (neuro worse), fusion brace

Normal

Bools and Rose, 1986 (4)

III

Normal

Traction, fusion brace

Normal

Collalto et al., 1986 (7)

Mixed I/lateral

Normal

None (neuro worse), fusion brace

Monoparesis

Putnam et al., 1986 (45)

Quadriplegia, CN 6

Brace

Death (sepsis 8 mo)

Normal

Ramsay et al., 1986 (46)

Quadriparesis

None (neuro worse), traction brace

Hemiplegia

Roy-Camille et al., 1986 (48)

CN 6, 11

None, brace failed (3 mo), traction fusion

CN 6

Quadriplegia, CN 6, 912

Traction fusion

Quadriplegia

Zigler et al., 1986 (57)

Quadriplegia, CN 11

Traction brace fusion

Quadriplegia

Watridge et al., 1985 (52)

Lateral

Paraparesis

None (neuro worse), traction fusion

Normal

decompression brace
Banna et al., 1983 (2)

Rotatory

Normal

Traction (2 wk)

Kaufman et al., 1982 (31)

II

Quadriplegia

Brace fusion

Quadriparesis, CN 9, 10

II

Monoparesis

Brace

Normal

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Guidelines for Management of Cervical Spinal Injuries

TABLE 14.2. Continued


Series (Ref. No.)
Woodring et al., 1981 (54)

Type

Initial Examination

Treatment

Outcome

Hemiparesis, CN 6

Traction

Monoparesis

None (neuro worse), traction fusion

CN 6
Quadriplegia

Powers et al., 1979 (43)

Hemiparesis, CN 6

Traction brace

Hemiparesis

II

Hemiparesis, CN 7

Traction brace

Normal

Rockswold and Seljeskog, 1979 (47)

II

Hemiparesis, CN 6

Traction, brace fusion

Ambulates

Eismont and Bohlman, 1978 (13)

III

Normal

Collar (neuro worse), fusion brace

Normal

Fruin and Pirotte, 1977 (18)

Hemiparesis, CN 6, 912

Traction fusion

CN 6, 11

Page et al., 1973 (39)

Quadriplegia, CN 10, 12

Traction, brace failed (5 mo), fusion

Quadriparesis, CN 10

Evarts, 1970 (14)

Hemiparesis, CN 6, 9, 10, 12

Traction, brace fusion

CN 6

Gabrielsen and Maxwell, 1966 (19)

Hyperreflexic, CN 6

Traction, brace failed (3 mo), fusion

Numb scalp

Farthing, 1948 (16)

III

Normal

Traction brace

Normal

Three articles were eliminated because the type of dislocation was not reported: Georgopoulos et al. (20) (2 of 3 patients); Bulas et al. (5)
(5 of 5 patients); Naso et al. (37) (1 of 2 patients). Two articles (8 patients) were eliminated because the initial examination was not reported:
Grabb et al. (21) (3 patients); Ahuja et al. (1) (5 patients). Two articles (6 patients) were eliminated because the treatment was not reported: Maves
et al. (35) (3 patients); Hladky et al. (26) (3 patients). Two articles were eliminated because the outcome was not reported: Jones et al. (30) (1
patient); Bools and Rose (4) (1 of 2 patients). CN, cranial nerve; neuro, neurological examination.

follow-up (2, 4, 16, 33). The remaining 15 patients had improved neurological function compared with their initial findings at last follow-up (3, 6, 14, 15, 18, 19, 36, 39, 43, 47, 48, 54,
57). Ten had Type I injuries, five had Type II injuries, two had
Type III injuries, and two had other dislocations. In total, one
of six patients with Type II injuries and one of three patients
with other translational injuries had transient worsening with
the use of craniocervical traction. In summary, traction for
AOD has been reported to cause occasional neurological
worsening. In both circumstances, the worsening did not
persist after discontinuation of traction. Because the frequency of neurological worsening with traction for AOD is
approximately 10%, 10 times higher than for subaxial injuries,
the use of traction should be considered with caution in
patients with AOD.
Of 19 patients initially treated with external immobilization
excluding traction, 8 patients were immobilized in anticipation of internal fixation and fusion and none worsened during
the presurgical interval (one Type I, four Type II, three other
type) (10, 11, 31, 33, 38, 44). Of the remaining 11 patients
treated with external immobilization alone excluding traction,
4 worsened transiently (three Type I, one Type II) (9, 11, 13,
27). All subsequently underwent craniocervical fixation and
fusion. Two of these patients were normal at follow-up (one
initially normal, one initially hemiparetic), and two were
spastic (one initially quadriparetic and one hemiparetic). Of
the remaining seven patients managed with external immobilization alone who did not worsen while in external immobilization, two patients managed in collars and one patient
treated in a halo were unstable after 6 to 22 weeks of immobilization (one Type I, two Type II). Two were quadriplegic,
and one was normal. All three underwent internal fixation
and fusion without change in their initial neurological condition at last follow-up. Only four patients with AOD were
successfully treated with external immobilization alone (one
Type I, two Type II, one other dislocation). Of the 21 patients
initially treated with traction, 6 were subsequently managed
with external immobilization and none developed neurolog-

ical worsening. Two of the six (both Type I) remained unstable after 3 to 5 months of bracing and were subsequently
treated with craniocervical fixation and fusion. Five of those
six patients had improvement in their neurological condition
at follow-up. The sixth patient remained normal.
In summary, 5 of 13 patients with AOD who did not worsen
neurologically while treated with external immobilization
(with or without traction) failed to achieve bony union with
stability without internal fixation and fusion. In addition, six
patients transiently worsened with external immobilization
(with or without initial traction). Factors affecting fusion or
persistent nonunion (e.g., degree and type of displacement,
patient age, and association with occipital condyle fractures)
could not be identified. Because 11 (28%) of 40 patients managed with external immobilization either deteriorated neurologically or failed to achieve craniocervical stability without
surgical internal fixation and fusion, treatment of AOD with
external immobilization alone should be considered with
caution.
Finally, 19 patients in the literature were treated with
planned early craniocervical fusion with internal fixation.
Only one patient worsened neurologically after surgery. This
patient with a Type II injury was normal initially and developed a Cranial Nerve X deficit that persisted at follow-up (44).
All but 3 of the remaining 18 patients improved neurologically at follow-up. Four had Type I, 10 had Type II, and 4 had
other types of dislocation. None of the patients treated with
craniocervical fusion and internal fixation had late instability
requiring reoperation or further treatment.

SUMMARY
AOD is an uncommon traumatic injury that is difficult to
diagnose and is frequently missed on initial lateral cervical
x-rays. Patients who survive often have neurological impairment, including lower cranial neuropathies, unilateral or bilateral weakness, or quadriplegia. But nearly 20% of patients

Neurosurgery, Vol. 50, No. 3, March 2002 Supplement

Traumatic Atlanto-occipital Dislocation Injuries

S111

FIGURE 14.1. Midsagittal diagrams of the


craniocervical junction show the various
methods for identifying AOD on a lateral
cervical x-ray. A, the Wholey measure; B,
the Powers ratio; C, the Dublin measure; D,
the X-line method; E, the BAI-BDI method.
with acute traumatic AOD will have a normal neurological
examination on presentation. The lack of localizing features
may impede diagnosis in the patient with a normal cervical
x-ray. A high index of suspicion must be maintained to diagnose AOD. Prevertebral soft tissue swelling on a lateral cervical x-ray or craniocervical subarachnoid hemorrhage on
axial CT has been associated with AOD and may prompt
consideration of the diagnosis. Additional imaging, including
CT and MRI, may be required to confirm the diagnosis of
AOD if plain x-rays are inadequate. All patients with AOD
should be treated. Without treatment, nearly all patients developed neurological worsening, and some did not recover.
Although treatment with traction and external immobilization has been used successfully in some patients, transient or
permanent neurological worsening and late instability have
been reported more often in association with these treatments
than with surgical treatment. Consequently, craniocervical
fusion with internal fixation is recommended for the treatment of patients with acute traumatic AOD.

KEY ISSUES FOR FUTURE INVESTIGATION


Although the use of external immobilization for AOD was
often associated with late instability, several patients achieved
stability without operative management. CT with threedimensional reconstruction for more precise measurement of

the magnitude of displacement and MRI for differentiation of


partial and complete ligament tears from stretch injuries may
be useful in identifying a subgroup of patients in whom
stability might be achieved with external immobilization
alone. Because AOD remains relatively infrequent, cooperative prospective collection of plain radiographic, computed
tomographic, and MRI data in patients with AOD is recommended to determine whether a subgroup of patients with
AOD can be treated with external immobilization alone with
fewer occurrences of late instability.
Reprint requests: Mark N. Hadley, M.D., Division of Neurological
Surgery, University of Alabama at Birmingham, Division of Neurological Surgery, 516 Medical Education Building, 1813 6th Avenue
South, Birmingham, AL 35294-3295.

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Drawings by Leonardo da Vinci. Courtesy, Dr. Edwin Todd, Pasadena, California.